Abstract

Abstract Background and Aims Presepsin is a soluble CD14 subtype known as a sepsis biomarker. Recently, it has been reported to correlate with kidney function decline in elderly patients with chronic kidney disease and to predict acute kidney injury in patients with sepsis. However, the potential role of presepsin in systemic lupus erythematosus (SLE) with kidney involvement is still unclear. This study aimed to evaluate the relationship between serum presepsin level and SLE disease activity and laboratory parameters and to validate presepsin as a biomarker for lupus nephritis (LN). Method This cross-sectional study included 78 SLE patients aged 38.9±12.8 years. Among them, there were 68 (87.2%) women, 36 (46.2%) patients with LN, and 42 (53.8%) patients without LN. LN was diagnosed by renal biopsy and/or according to the renal SLE disease activity index (SLEDAI) criteria. Patients with infections were not included in the study. Serum presepsin level was determined by ELISA. The diagnostic value of presepsin level for the detection of LN was assessed by receiver-operating characteristic curves (ROC), the area under the curve (AUC), and 95% confidence intervals (CI). Spearman and Pearson correlation tests were performed to evaluate the relationships between presepsin level and SLEDAI score, serum complement concentrations, anti-double-stranded DNA antibodies (anti-dsDNA), inflammatory markers, urinary protein, and estimated glomerular filtration rate (eGFR) with CKD-EPI. Results The median serum presepsin level was significantly higher in patients with LN than in those without kidney damage [145 (110-197) pg/ml vs 102 (82-146) pg/ml, p = 0.011]. The ROC analysis found that the most appropriate cut-off point for presepsin concentration as a biomarker for LN in LSE patients was 106 pg/ml with a sensitivity of 81.8% (95% CI 64.5-93.0), and specificity of 54.3% (95% CI 36.6-71.2). The AUC was 0.714 (95% CI 0.592-0.837) with a positive predictive value of 62.8% (95% CI 46.7-77.0), and a negative predictive value of 76.0% (95% CI 54.9-90.6) (Fig. 1). The mean value of eGFR was 83.8±27.0 ml/min/1.73 m2 in the LN group and 94.1±18.0 ml/min/1.73 m2 in the non-LN group (p = 0.112). A significant negative correlation was observed between presepsin levels and eGFR in LN patients (Fig. 2). Moreover, presepsin levels in the LN group significantly correlated with SLEDAI score (r = 0.372, p = 0.036), anti-dsDNA titer (r = 0.363, p = 0.04) and severity of proteinuria (r = 0.630, p<0.01). No such associations were found in SLE patients without kidney involvement. Presepsin concentration did not correlate with C3, C4, C-reactive protein, erythrocyte sedimentation rate, and procalcitonin levels in both groups. Conclusion Serum presepsin may be considered a potential biomarker for the detection of kidney damage in patients with SLE. Further studies focusing on the clinical and pathological associations of presepsin in LN would be of interest.

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